2018 ACOI Internal Medicine Board Review. Peripheral Vascular Disease. Robert Bender, DO, FACOI, FACC

Transcription

1 2018 ACOI Internal Medicine Board Review Peripheral Vascular Disease Robert Bender, DO, FACOI, FACC

2 Peripheral Vascular Disease (PVD) Arteriosclerosis Obliterans (ASO) Aneurysmal Disease Acute Arterial Occlusion Thromboangiitis Obliterans (Buergers Disease)

3 Arteriosclerosis Obliterans (ASO) v Overview: Manifestation of atherosclerosis 95% of chronic occlusive arterial disease Generalized disease of aorta and branches Slow progression

4 ASO v Demographics: Age > 50 years old Male > female x 2 1/3 have clinical CAD > 50% have severe CAD by cath Up to 1/3 = diabetic ¼ have sigificant carotid stenosis

5 v v ASO Risk Factors: Diabetes, smoking, HTN, Lipids, homocysteine Diabetes & Smoking = highest rel. risk Pathophysiology: Atheromatous plaque arterial narrowing complete arterial occlusion (due to plaque or thrombus) Tissue ischemia, collaterals

6 ASO v Clinical Claudication = muscle ischemia aorto-iliac disease = hips, thighs, buttocks femoral - popliteal disease = lower leg popliteal - tibial disease = foot Rest Pain Ulceration foot, toes = most common painful may progress to gangrene Acute Occlusion = thrombus, embolism

7 ASO - Clinical * Pulses = location of decreased pulse clue to site of stenosis * Ankle-Brachial index = ratio of DP or PT / highest brachial systolic BP = normal = borderline = abnormal < 0.4 = severe, indicates risk of development of critical limb ischemia *NB = may not correlate with symptoms Bruits = not indicative of degree of stenosis

8 ASO - Clinical v v v Skin color changes pallor with elevation reactive hyperemia (rubor) and delayed venous filling (>15 sec) with dependency Trophic changes: hair loss; dry, scaly skin cool foot + chronic hyperemia Ulcers: spontaneous, post-traumatic pale, painful, irregular border

9 ASO diagnostic tests ABI s = very sensitive (~90%) and specific (>95%) in detecting presence of PAD using 0.9 as a cut-off Exercise ABI s = may help to differentiate claudication from pseudoclaudication and to assess functional status in patient s with PAD Ultrasound = simple, inexpensive, location and severity, f/u CTA = pre-intervention MRA = pre-intervention Contrast Angiography = at time of intervention

10 ASO v Treatment 75% = stable course 25% = progressive * ¼ = amputation Critical Limb Ischemia (rest pain, tissue loss) = prompt eval for revasc Morbidity / Mortality = CAD, stroke

11 v ASO Treatment: Asymptomatic = risk factor mods (including statin tx), anti-platelet rx (class IIa), +/- ACEI, long term f/u Mild to moderate disease medical treatment = risk factor mod., ASA or clopidogrel (class I), Cilostazol (not with CHF/LV dysfunction) cornerstone = walking (supervised vs home program min > 3x/week) Severe or rapidly progressive disease endovascular intervention, surgery goal = symptom relief, functional improvement, limb salvage

12 Abdominal Aortic Aneurysm (AAA) v Overview: Defined = minimum A-P diameter > 3cm. Etio. = atherosclerosis (90-95%), hereditary, inflam, infect, aortopathy (Marfans, Bicuspid AV) Prevalence 2% of elderly 10% at autopsy in males > 60 y.o. males > females 5-8 x Most common arterial aneurysm 98% = infra-renal

13 AAA * Risk Factors = HTN, smoking,?familial * Progression = enlargement 1-4 mm/yr. (<4cm AAA) to 7-8 mm/yr (large) * Complications = rupture, thromboembolism, compression, erosion * 10% of patients with lower extrem. ASO have an AAA = so screening reasonable for AAA (class IIa) in pts with sx PAD

14 AAA v Clinical: Symptoms = with active enlargement or rupture Abdominal or back pain Less common G-I bleeding (d/t erosion) rupture into IVC lower extrem. emboli 90% ruptures = retroperitoneal Ominous triad = abdominal/back pain, pulsatile abdominal mass, low blood pressure

15 AAA-Clinical v Physical Exam: incidental finding pulsatile mass = epigastric 25% = bruit tenderness = pending rupture rupture = shock

16 AAA v Diagnostic tests: Abdominal x-ray = calcific outline Ultrasound = inexpensive, serial testing CT Angiography or MRA = pre-op testing

17 AAA v Pre-op Evaluation Pulmonary Cardiac Nuclear Stress/Persantine Cardiac Catheterization positive stress test symptomatic v Operative mortality = related to age and presence of CAD v Leading cause of Peri-Op Death = CAD

18 AAA * Monitoring < 4 cm = US q 2-3 yrs cm = US q 6-12 months * Surgery or endovascular repair Timing: Diameter > 5.5cm Size > 0.5cm/6 mos. Symptomatic = emergent Rupture = high mortality

19 Thoracic Aortic Aneurysm Abnormalities of Aortic Media Bicuspid Aortic Valve Marfan s Turner s Synd Loey s-dietz Synd Familial/non-syndromic screen pt. and 1 st degree relatives

20 Popliteal Artery Aneurysm 70% of all lower extrem aneurysms Can be bilateral Risk of AAA Complications: *distal emboli *thrombosis in-situ *rupture = uncommon Surgical repair = symptoms or > 2 cm dia

21 Acute Arterial Occlusion v Etiology = embolic, thrombotic, traumatic Embolic= Cardiac origin = 80-90% Afib = 75% LV thrombus Endocarditis Left atrial myxoma Non-Cardiac aortic plaque ulceration or disruption embolus from aneurysm paradoxical venous thrombo-embolism

22 Acute Arterial Occlusion v Etiology (continued): Thrombotic = ASO Lower extrem. Aneurysm (with thrombosis in-situ) Buergers disease/arteritis Local trauma Hypercoagulable states

23 Acute Arterial Occlusion v Clinical = 6 - P s Pain = rapid onset Polar (poikilothermia) = cold limb Pallor = with venous collapse progression to bluish mottling = tissue ischemia and necrosis Pulseless = Thrombus propagation with time Paresthesia = ischemic neuropathy May progress to complete loss of sensation and motor function Paralysis = ischemic nerve injury and muscle rigidity chance of limb salvage

24 Acute Arterial Occlusion v Pathophysiology: Release of K +, myoglobin, lactic acid = hyperkalemia, acidosis, renal failure Flow restoration = wash-out of K + and lactic acid, arrhythmia, hemo. Instability, post-revasc compartment syndrome.

25 Acute Arterial Occlusion v Differential Diagnosis = Phlegmasia cerulea dolens = acute extensive DVT Lower extrem. cyanosis, acute swelling, edema, leg vein distension, or absent pulses Ergotism Acute aortic dissection Low Cardiac - Output State in patient with preexisting ASO/stenosis = perfusion pressure

26 Acute Arterial Occlusion v Treatment = Heparin = prevent thrombus propagation * Unless category III / irreversible = amputation Rapid Evaluation and Revascularization = endovascular, surgery

27 Thromboangiitis Obliterans Buerger s Disease v v v v v Pathophysiology = inflam. occlusive disease of small and medium size peripheral arteries and veins in young male smokers Age of onset = < 50 y.o./freq. < 30 y.o. Absence of Risk Factors = except smoking > 90% male Prevalence mid and far-east

28 Buerger s Disease v Etiology = uncertain, but Smoking is related to progression or remission Cessation of smoking = improved prognosis Continuation of smoking = disease progression Ischemic symptoms = distal extrems.

29 Buergers Disease v Clinical = Claudication instep of foot hand = writers cramp Numbness/paresthesias, Raynauds Ulceration, gangrene Thrombophlebitis = superficial or deep classically migrating and transient ( phlebitis migrans )

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32 Buerger s Disease v Treatment STOP SMOKING Surgical revascularization = generally dismal long term results Sympathectomy (thoracic, lumbar) = symptom relief Amputation = gangrene, severe infection, debilitating pain Growth Factor angiogenesis =?